Overview
Dr. Kastan earned his M.D./Ph.D. from Washington University School of Medicine and did his clinical training in Pediatrics and Pediatric Hematology-Oncology at Johns Hopkins. He was a Professor of Oncology at Johns Hopkins prior to becoming Chair of the Hematology-Oncology Department and later Cancer Center Director at St. Jude Children’s Research Hospital, before moving to Duke in 2011, where he currently serves as the Executive Director of the Duke Cancer Institute and is the William and Jane Shingleton Professor of Pharmacology and Cancer Biology. His laboratory research has focused on cellular responses to DNA damage, including many highly cited publications reporting the roles of p53 and ATM in DNA damage signaling. Among his numerous honors are election to the National Academy of Sciences, National Academy of Medicine, and the American Academy of Arts and Sciences, and receipt of the AACR-G.H.A. Clowes Memorial Award and Failla Award from the Radiation Research Society. He has served as Chair of the Board of Scientific Counselors of the National Cancer Institute (NCI), on the Boards of Directors of the American Association for Cancer Research (AACR) and the American Association of Cancer Institutes (AACI), and as Editor-in-Chief of the journal Molecular Cancer Research. His lab continues to study molecular and biochemical controls of cellular stress responses, particularly those related to DNA damage, and has spun out two companies focused on novel anti-cancer therapeutics.
Current Appointments & Affiliations
Recent Publications
ATM interaction with GRP94 modulates oncogenic receptor expression and signaling and microglial activation.
Journal Article Proc Natl Acad Sci U S A · December 30, 2025 Ataxia-telangiectasia (A-T), caused by biallelic mutations in the ATM gene, leads to multiple disease phenotypes, including cerebellar neurodegeneration, radiosensitivity, cancer predisposition, immunodeficiency, insulin resistance, and pulmonary inflammat ... Full text Link to item CiteA Novel Dual ATM/DNA-PK Inhibitor, XRD-0394, Potently Radiosensitizes and Potentiates PARP and Topoisomerase I Inhibitors.
Journal Article Mol Cancer Ther · June 4, 2024 A majority of patients with cancer receive radiotherapy as part of their treatment regimens whether using external beam therapy or locally-delivered radioisotopes. While often effective, some tumors are inadequately controlled with radiation and radiothera ... Full text Link to item CiteFigure S5 from A Novel Dual ATM/DNA-PK Inhibitor, XRD-0394, Potently Radiosensitizes and Potentiates PARP and Topoisomerase I Inhibitors
Other · June 4, 2024 <p>Plasma concentrations</p> ... Full text CiteRecent Grants
Pharmacological Sciences Training Program
Inst. Training Prgm or CMEPreceptor · Awarded by National Institutes of Health · 2025 - 2030Cancer Center Support Grant (CCSG)
ResearchPrincipal Investigator · Awarded by National Institutes of Health · 1976 - 2029Modulation of the A-T Phenotype via GRP94
ResearchPrincipal Investigator · Awarded by Ataxia Telangiectasia Children's Project, Inc · 2025 - 2028View All Grants